22.6A ).Atthestartofexhalationthedrivingpressureforexpiratorygasflowisthesameasinanormalindividual;thatis,thedrivingpressureisthesumoftheelasticrecoilpressureandpleuralpressure.Asexhalationproceeds,however,theresistivedropinpressureisgreaterthaninthenormalindividualbecauseofthegreaterdecreaseinairwayradiussecondarytotheaccumulationofmucusandtheinflammation.Asaresulttheequalpressurepointnowoccursinsmallairwaysthataredevoidofcartilage.Theseairwayscollapse.Thiscollapseisknownaspremature airway closure, whichresultsinaless-than-maximalexpiratoryvolumeandproducesanincreaseinlungvolumeknownasair trapping.Theincreaseinlungvolumeinitiallyhelpsoffsettheincreaseinairwayresistancecausedbytheaccumulationofmucusandinflammationbecauseitresultsinanincreaseinairwaycaliberandelasticrecoil.Asthediseaseprogresses,however,inflammationandaccumulationofmucusincreasefurther,thereisagreaterincreaseinexpiratoryresistance,andmaximalexpiratoryflowratesdecrease.
Fig.22.6B ).Atthestartofexhalationthedrivingpressureforexpiratorygasflowisreducedsecondarytoalossofelasticrecoil.Whiletheresistivedropinpressureisnormal,thesmallerinitialdrivingpressureresultsinanequalpressurepointthatoccursclosertothealveolusinairwaysthatdonotcontaincartilage.Prematureairwayclosureagainoccursbutforaverydifferentreasonthantheprematureairwayclosureobservedinindividualswithanincreaseinairwayresistance.
Individualswithprematureairwayclosurefrequentlyhavecrackles, alsosometimescalledrales, apoppingsoundusuallyheardduringinspirationonauscultation.Thesecracklesareduetotheopeningofairwaysduringinspirationthatclosed(i.e.,werecompressed)duringthepreviousexhalation.Cracklescanbeduetomucusaccumulation,airwayinflammation,fluidintheairways,oranymechanismresponsibleforairwaynarrowingorcompression.Theyarealsoheardinindividualswithemphysema,inwhichthereisadecreaseinlungelasticrecoil.Infact,acuteandchroniclungdiseasescanchangetheexpiratoryflow-volumerelationshipbychangesin(1)staticlungrecoilpressure,(2)airwayresistanceandthedistributionofresistancealongtheairways,(3)lossofmechanicaltetheringofintraparenchymalairways,(4)changesinthestiffnessormechanicalpropertiesoftheairways,and(5)differencesinseverityoftheaforementionedchangesinvariouslungregions.
mean dynamic compliance of the lung (dyn CL) is calculated as the slope of the line that joins the end-inspiratory and end-expiratory points of no flow (
Fig. 22.7
Dynamic compliance is always less than static compliance, and it increases during exercise. This is because during tidal volume breathing, a small change in alveolar surface area is insufficient to bring additional surfactant molecules to the surface, and thus the lung is less compliant. During exercise the opposite occurs; there are large changes in
Mucus, Edema, Bronchoconstriction PL = 90˜60 = 30 cm H2O
Fig. 22.6 A,Flowlimitationinthepresenceofincreasedairwayresistance.B,Flowlimitationinthepresenceofalossofelasticrecoil.